The term “eczema,” often used to describe atopic dermatitis, was coined in ancient Greece, and roughly translates as “to boil out.” Modern science, however, recognizes the contribution of both host and environmental factors to this disease. Hallmarks of the disease include reduced barrier function, reduced innate immune activation, and susceptibility to infections with Staphylococcus aureus. Predisposing host factors are suggested by monogenic mutations in STAT3, filaggrin, and other genes associated with AD-like phenotypes (Lyons et al., Immunology and allergy clinics of North America 35, 161-183 (2015); published online Epub February (10.1016/j.iac.2014.09.008)). Host genetic influences can be therapeutically modulated through topical steroids or calcineurin inhibitors (Boguniewicz and Leung, J Allergy Clin Immunol 132, 511-512 e515 (2013); published online (Epub) August (10.1016/j.jaci.2013.06.030)). S. aureus contributes to AD pathogenesis, and can be mitigated by antibiotics (Boguniewicz and Leung, supra; Kobayashi et al., Immunity 42, 756-766). Recent work has revealed that the skin microbiome is significantly different between healthy controls and patients with AD and that symptoms are associated with a loss of commensal diversity (Kong et al., Genome research 22, 850-859 (2012); published online (Epub) May (10.1101/gr. 131029.111)). A need remains for methods for therapeutically targeting this dysbiosis and treating atopic dermatitis.